Pathological findings underlying focal temporal lobe hypometabolism in partial epilepsy

TLDR

Focal temporal lobe hypometabolism seen on PET often lacks corresponding histopathological lesions, suggesting submicroscopic structural changes or functional neuronal alterations. The study examined temporal lobe tissue from 25 patients with partial complex seizures who had interictal FDG‑PET scans and then underwent anterior temporal lobe resection. PET hypometabolism was present in 22 of 25 patients and matched focal pathology in 19 cases (15 mesial temporal sclerosis, 2 neoplasms, 1 angioma, 1 heterotopia), with the extent of hypometabolism generally exceeding the histological lesion and correlating with lesion severity, while a few PET abnormalities were transient or located beyond the resected area.

Abstract

Abstract Histopthogical studies were carried out on temporal lobe tissue from 25 patients with partial complex seizures who were studied by interictal positen computed tomography (PCT) with 18 F‐fluorodeoxyglucose and subsequently underwenty anterior lobe resection. Abnormalities were identified on x‐ray computed tomographic scane in 7 patients, but none indicated the site of a pathologically confirmed structural lesion. Hypometabolic zones were observed on PCT scans of 22 patients and corresponded to focal pathological abnormalities in 19 (15 mesial temporal sclerosis, 2 small neoplasms, 1 angioma, 1 heterotopia). In 1 patient with a foclly abnormal PCT scan and no pathological changes, the lesion may have been located posterior to the resection. In the remaining 2 patients, the hypometabolic zones later disappeared and may have represented a transient response reponse induced by depth electrode implantation. Three patients with normal PCT scans had no pathological abnormalities in their resected tissue. The degree of relative hypometabolism measured by PCT correlated well with the severity of the pathological lesion, byt the size of the hypometabolic zone was generally much larger than the area of pathological involvement. This discrepancy could not be considered an artifact of techique and muist represent either structural abnormalities below the resolution of routine histopathological studies (e.g., loss of synapses) or functional incativation of neuronal elements associated with the epileptogenic lesion.